Dietary restriction suppresses apoptotic cell death, promotes Bcl-2 and Bcl-xl mRNA expression and increases the Bcl-2/Bax protein ratio in the rat cortex after cortical injury

Lončarević-Vasiljković, Nataša; Milanović, Desanka; Pešić, Vesna; Tešić, Vesna; Brkic, Marjana; Lazić, Divna; Avramovic, Vladimir; Kanazir, Selma

doi:10.1016/j.neuint.2016.02.017

Cited by 31 publications

(23 citation statements)

References 28 publications

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“…Caspase-3 is the key mediator of cell apoptosis and has a role in a variety of apoptotic signaling pathways (33–35). Previous studies have reported that overexpression of Bcl-2 can effectively inhibit the activation of caspase-3, thus inhibiting the occurrence of apoptosis (36). In the present study, RT-qPCR and western blotting revealed that EVI-1 overexpression/silencing altered the expression of the aforementioned proteins associated with apoptosis, and subsequently the process of apoptosis, in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

EVI‑1 acts as an oncogene and positively regulates calreticulin in breast cancer

Wang

et al. 2018

Mol Med Report

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Ecotropic viral integration site-1 (EVI-1) is an important transcription factor involved in oncogenesis. Aberrant EVI-1 expression has been reported to be a characteristic of multiple types of malignancies; however, very little is known about how EVI-1 regulates breast cancer. Current knowledge of how target genes mediate the biological function of EVI-1 remains limited. In the present study, overexpression of EVI-1 promoted cell proliferation, migration, and invasion, and inhibited apoptosis in breast cancer. By contrast, silencing of EVI-1 inhibited cell proliferation, migration and invasion, and enhanced apoptosis in breast cancer. In addition, the results also revealed that the aberrant expression of EVI-1 regulates genes associated with the apoptotic pathway in breast cancer. Furthermore, EVI-1 was also likely to target the promoter region of calreticulin (CRT) in vitro . It was concluded that EVI-1 can affect epithelial mesenchymal transition-associated genes by regulating the expression of CRT in breast cancer. The results revealed that EVI-1 may be a potential effective therapeutic target in breast cancer.

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Section: Discussionmentioning

confidence: 99%

EVI‑1 acts as an oncogene and positively regulates calreticulin in breast cancer

Wang

et al. 2018

Mol Med Report

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“…Moreover, CR was found protective in conditions of brain injury (Loncarevic-Vasiljkovic et al 2016; Mychasiuk et al 2015). Thus, the main goal of the present study was to assess the cognition-sparing effects of two different DR regimens, IF and CR, in closed-head mTBI mouse model.…”

Section: Discussionmentioning

confidence: 97%

“…IF is neuroprotective and neurorestorative in a wide range of animal models of brain injury and neurodegenerative disorders (Mattson 2012). DR was previously shown to protect neurons and improve functional outcome in animal models of stroke, epilepsy, and TBI when initiated prior to the brain injury (Arumugam et al 2010; Bruce-Keller et al 1999; Fann et al 2014; Loncarevic-Vasiljkovic et al 2016; Loncarevic-Vasiljkovic et al 2012; Rich et al 2010). In the present study, we show that IF and CR are effective in ameliorating cognitive deficits in a mTBI model when initiated after the brain injury.…”

Section: Discussionmentioning

confidence: 99%

Dietary Energy Restriction Ameliorates Cognitive Impairment in a Mouse Model of Traumatic Brain Injury

et al. 2019

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Traumatic brain injury (TBI) is one of the most common causes of neurological damage in young people. It was previously reported that dietary restriction, by either intermittent fasting (IF) or daily caloric restriction (CR), could protect neurons against dysfunction and degeneration in animal models of stroke and Parkinson’s disease. Recently, several studies have shown that the protein Sirtuin 1 (SIRT1) plays a significant role in the induced neuroprotection following dietary restriction. In the present study, we found a significant reduction of SIRT1 levels in the cortex and hippocampus in a mouse model of mild weight-drop closed head TBI. This reduction was prevented in mice maintained on IF (alternate day fasting) and CR initiated after the head trauma. Hippocampus-dependent learning and memory (measured using a novel object recognition test) was impaired 30 days post-injury in mice fed ad libitum, but not in mice in the IF and CR groups. These results suggest a clinical potential for IF and/or CR as an intervention to reduce brain damage and improve functional outcome in TBI patients.

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“…Upregulation of caSR leads to changes in the expression of AIF, Bcl-2 and Bax that serve a key role in regulating the mitochondrial pathway of apoptosis (59,60). To gain additional insights into the association between apoptosis and the activation of caSR during cIRI, the intracellular and extracellular concentration of calcium was detected in OGd/R Pc12 cells subjected to Astragaloside IV, Gdcl 3 (a specific CaSR agonist), NPS-2143 (a specific CaSR antagonist) or a combination of Astragaloside IV and Gdcl 3 treatments, and the protein expression of AIF, Bcl-2 and Bax in vitro was analyzed.…”

Section: Discussionmentioning

confidence: 99%

Astragaloside IV attenuates cerebral ischemia‑reperfusion injury in rats through the inhibition of calcium‑sensing receptor‑mediated apoptosis

Zhang

Zhao

et al. 2020

Int J Mol Med

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cerebral ischemia-reperfusion injury (cIRI), caused by the reperfusion of blocked vessels following ischemic stroke, can lead to secondary brain injury. Throughout cIRI, apoptosis serves an important role. Astragaloside IV is a potential neuroprotectant that alleviates cIRI by inhibiting apoptosis. The calcium-sensing receptor (caSR) is a G-protein-coupled receptor, the activation of which aggravates ischemia-reperfusion injury. The aim of the present study was to investigate whether the protective effect of Astragaloside IV on cIRI may be associated with the regulation of caSR. A rat middle cerebral artery occlusion/reperfusion (McAO/R) model and an oxygen and glucose deprivation/reoxygenation (OGd/R) model of pheochromocytoma (Pc12) cells were used to study the neuronal injury induced by cIRI. Neurological function scores (NFS), 2,3,5-triphe-nylterazolium chloride and hematoxylin and eosin staining were used to determine brain damage in rats. cell viability was measured to evaluate the injury of OGd/R Pc12 cells. Western blotting was used to examine the expression of proteins associated with apoptosis and caSR. The caSR antagonist NPS-2143 and agonist Gdcl 3 were used to further confirm the effects of caSR during the process of apoptosis. The results demonstrated that Astragaloside IV alleviated cIRI by decreasing the NFS of rats, reducing the infarction volume of the brain and promoting the viability of Pc12 cells, as well as inhibiting the expression of cleaved caspase-3 and caSR, which was induced by cIRI. The results of the present study suggested that the activation of caSR may be involved in cIRI-induced brain damage in rats, and that Astragaloside IV may alleviate cIRI by inhibiting caSR activation-induced apoptosis.

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Dietary restriction suppresses apoptotic cell death, promotes Bcl-2 and Bcl-xl mRNA expression and increases the Bcl-2/Bax protein ratio in the rat cortex after cortical injury

Cited by 31 publications

References 28 publications

EVI‑1 acts as an oncogene and positively regulates calreticulin in breast cancer

EVI‑1 acts as an oncogene and positively regulates calreticulin in breast cancer

Dietary Energy Restriction Ameliorates Cognitive Impairment in a Mouse Model of Traumatic Brain Injury

Astragaloside IV attenuates cerebral ischemia‑reperfusion injury in rats through the inhibition of calcium‑sensing receptor‑mediated apoptosis

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